MBD2 and SOCS3 regulate Th17 cells and the pathogenesis of severe asthma
MBD2与SOCS3调控Th17细胞与重症哮喘发病机制

摘要

哮喘是一种具有较大差异性的炎性疾病，主要源于炎性细胞和其触发的细胞因素，该疾病会造成长期的气道炎症。哮喘在支气管中的频率较高，这种疾病通常伴随着气道炎症。大多数哮喘患者的病情无法得到有效的治疗，最终会演变为重症哮喘。该疾病的显著症状包括气道的再塑性和气道的反向阻塞，这种疾病的产生大多源自于吸入的过敏物质，并且会导致一系列哮喘相关的症状，例如呼吸困扰、咳嗽、气喘，还有因气道收缩导致的喘息，从而产生哮喘的哮鸣声。在对哮喘的形成原理的深入研究里，免疫失衡以及其相应的学术研究起到了关键性作用。本文将对甲基CpG结合蛋白2（MBD2）和细胞因子信号传导抑制蛋白3（SOCS3）如何影响辅助性T细胞17（Th17）细胞对于严重哮喘的影响的最新研究成果进行综述讨论。

Abstract

Asthma is a very heterogeneous inflammatory disease, mainly due to inflammatory cells and their triggering cellular factors, the disease will cause long-term airway inflammation. Asthma in the bronchial frequency is higher, the disease is usually accompanied by airway inflammation. Most of the asthma patients can not be effectively treated, and eventually will evolve into severe asthma. The significant symptoms of the disease include airway remodeling and airway reverse obstruction, the disease is mostly produced by inhaled allergenic substances, and will lead to a series of asthma-related symptoms, such as respiratory distress, cough, wheezing, and wheezing caused by airway contraction, resulting in asthma wheeze. In the in-depth study of the formation principle of asthma, immune imbalance and its corresponding academic research plays a key role. This article will review the latest research results on how methyl CpG binding protein 2 (MBD2) and cytokine signaling inhibitor 3 (SOCS3) affect helper T cell 17 (Th17) cells for severe asthma.